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These findings demonstrate the importance of LTbetaR signaling in leukocyte migration.
our study clarifies the epithelial intrinsic role of LTbR on medullary thymic epithelial cells development and function; more importantly, it reveals a previously unrecognized function of LTbR on the control of the size of medullary thymic epithelial cells progenitor population.
LTbetaR is required for T-cell regeneration on irradiation-induced thymic injury.
Regulatory T-lymphocytes engage lymphotoxin beta receptor for afferent lymphatic transendothelial migration to preserve the survival of a pancreatic islet graft.
Low LTBR expression is associated with Herpes Simplex.
The LIGHT (Tumour necrosis factor ligand superfamily member 14, TNFSF14)/Lymphotoxin beta-Receptor(LTbeta-R) pathway, which is involved in T-cell and macrophage activation, was diminished in plasma and in apoE-/-Irs2+/-HL-/- atheromas.
Data indicate that thymus medulla specialization for thymic tolerance segregates from medulla organogenesis and instead involves lymphotoxin beta receptor (LTbetaR)-mediated regulation of the thymic dendritic cells (DCs) pool.
EAE induced by weak activation of innate immunity requires the NLRP3 inflammasome and is sensitive to interferon-beta treatment
lymphatic vessel expansion occurs in two distinct phases; the first wave of expansion is dependent on IL-7; the second phase, responsible for leukocyte exit from the glands, is regulated by lymphotoxin (LT)betaR signaling
Data show that growth of regenerating splenic tissue is suppressed by lymphotoxin beta-receptor (LTbetaR) expression at non-splenic sites.
LTbetaR is essential for efficient liver regeneration and cooperates with TNFRp55 in this process. Differences in survival kinetics strongly suggest distinct functions for these two cytokine receptors in liver regeneration.
our results reveal a novel role for LTbetaR signaling in epithelial cells in the regulation of intestinal epithelial cell homeostasis to limit mucosal damage.
expression on artery tertiary lymphoid organs protects against atherosclerosis in aged mice
DC-derived LTBR ligands are critical mediators of lymph node cells survival, and LTBR signaling on reticular stromal cells is mediated by Pdpn expression.
LTbR plays a role in macrophage-driven inflammation in atherosclerotic lesions from ApoE knockout mice, probably by augmenting the Ccl5-mediated recruitment of monocytes.
M1 macrophages as inducer cells that trigger the expression of chemokines by vascular smooth muscle cell independently of lymphotoxin beta receptor signalling
lymphotoxin beta receptor regulates the development of the CCL21-expressing subset rather than the Aire-expressing subset of postnatal Medullary thymic epithelial cells.
found that conditionally LTbetaR-deficient animals failed to develop a significant proportion of their peripheral lymph nodes
LTbetaR activation on mouse macrophages is involved in the control of pro-inflammatory cytokine and mediator expression by activation of a signalling pathway that controls exacerbating inflammatory cytokine production.
LTbetaR activation on macrophages controls the pro-inflammatory response by activation of a TRIM30alpha-dependent signaling pathway
the lymphotoxin beta receptor (LTbetaR) to elicit the fast release of NF-kappaB inducing kinase (NIK) from the receptor complex leading to non-canonical NF-kappaB signaling.
these results suggest that the LTBR rs12354 polymorphism might be associated with the spontaneous resolution of hepatitis B virus infection
LTBR and BCLAF1 showed higher DNA methylation percentages in the marsupialized OKCs, but this difference did not affect gene expression (P > .05).
membrane-bound lymphotoxin-beta receptor (LTbetaR) and CXC chemokine receptor 2 (CXCR2), is involved in type B EAE development
LIGHT and LTBR interaction increases the survival and proliferation of human bone marrow-derived mesenchymal stem cells, and therefore, LIGHT might play an important role in stem cell therapy.
We found that LTbetaR polymorphisms caused severe BPH. Thus, LTbetaR may contribute to the risk of BPH development.
activation enhances the LPS-induced expression of IL-8 through NF-kappaB and IRF-1
LIGHT, via LTbetaR signaling, may contribute to exacerbation of airway neutrophilic inflammation through cytokine and chemokine production by bronchial epithelial cells.
Relative expression of HVEM and LTbetaR modulates canonical NF-kappaB and pro-apoptotic signals stimulated by LIGHT.
Dimerization of LTbetaR by LTalpha1beta2 is necessary and sufficient for signal transduction.
Studies indicate roles for Lymphotoxin-alpha (LTalpha) and lymphotoxin-beta receptor (LTbetaR) pathway in innate and adaptive immune responses to microorganisms.
Results suggest that blockade of lymphotoxin-beta receptor (LTBR) pathways may have therapeutic potential for treatment of Sjogren's syndrome.
LTBR gene polymorphisms may be associated with risk of IgA nephropathy in Korean children
Kidney-Tonifying plus Blood-Promoting Recipe regulates CD11b/CD18 and Bcl-2/Bax expression in blood leukocytes and improves microcirculatory status in aged patients with kidney deficiency and blood stasis syndrome.
show that a cognate interaction between LTalphabeta on CD4(+) helper T cells and LTbeta receptor on DCs results in unique signals that are necessary for optimal CD8(+) T-cell expansion via a type I IFN-dependent mechanism
These results indicated that AdipoR1 interacted with LTBR and mediated the inhibition of LTBR-activated NF-kappaB pathway.
LTbetaR levels are independently associated with atherosclerosis in multiple vascular beds
Increased potential for LTbeta receptor signaling, coupled with increased bioavailability due to lower decoy receptor-3 (DcR3) avidity, provides a mechanism for polymorphic variants in LIGHT to contribute to the pathogenesis of inflammatory diseases.
the LTbetaR modifies the ubiquitin:NIK E3 ligase, and also acts as an allosteric regulator of the ubiquitin:TRAF E3 ligase
This gene encodes a member of the tumor necrosis factor receptor superfamily. The major ligands of this receptor include lymphotoxin alpha/beta and tumor necrosis factor ligand superfamily member 14. The encoded protein plays a role in signalling during the development of lymphoid and other organs, lipid metabolism, immune response, and programmed cell death. Activity of this receptor has also been linked to carcinogenesis. Alternatively spliced transcript variants encoding multiple isoforms have been observed.
lymphotoxin B receptor
, tumor necrosis factor receptor superfamily member 3
, LT beta-R
, LT-beta receptor
, TNF receptor-related protein
, lymphotoxin-beta receptor
, tumor necrosis factor receptor superfamily, member 3
, tumor necrosis factor C receptor
, tumor necrosis factor receptor 2-related protein
, tumor necrosis factor receptor type III